Although we could not provide an explanation for why ADRP expression and hepatic lipid deposition were suppressed so strongly by ICAE treatment, we can only conclude that the protective effects of ICAE on fatty liver are concerned with the downregulation of PPARγ and ADRP protein expression, the suppression of ADRP is at least partly related to the downregulation of PPARγ expression, and other mechanisms might exist to account for the antifatty liver effects of ICAE. The gene discussed is PLIN2; the disease is fatty liver disease.